Effect of Rifampicin and Isoniazid on Liver Function

Lal, S.; Singhal, Smitha; Burley, Denis; Crossley, George H.

doi:10.1136/bmj.1.5793.148

Cited by 56 publications

(12 citation statements)

References 11 publications

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“…Because of the large number of elevations of enzyme activities and the good prognosis we thought liver biopsies unjustified in our patients, Since the timing of the rise in ASAT and ALAT activities varied greatly, monitoring of liver function should continue at regular intervals throughout therapy. Visudhipan and Chienchanya [15] reported a decline in transaminase values to a normal level within one week of reduction of the RP dosage, but Lal et al found the duration of elevated ASAT values was six to 24 days, irrespective as to whether the treatment was interrupted or not [9]. This was also true in our series, except that the time taken for the ASAT activities to return to normal was not dependent on the initial rise in the enzyme activity.…”

Section: Discussionsupporting

confidence: 56%

“…In earlier papers the frequency of patients with elevated transaminases is about 30%, so that our finding of a rise in 83% of patients is high [9]. One might therefore suspect that children are more sensitive to hepatic injury during RP and INH combination chemotherapy than adults.…”

Section: Discussionmentioning

confidence: 58%

“…However, its sideeffects are sometimes problematic in adults [7,12]. Transient elevation of serum transaminases have often been obtained during the early weeks of therapy [7,8,9]. Usually RP is combined with isoniazid (INH), which can also be hepatotoxic on its own [5,7,8].…”

Section: Introductionmentioning

confidence: 99%

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Hepatotoxicity of rifampicin and isoniazid in children treated for tuberculosis

Linna

Uhari

1980

Eur J Pediatr

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In order to determine the hepatotoxicity of rifampicin in children treated for tuberculosis, a survey was performed of 18 children receiving this medicine in combination with isoniazid. Fifteen of the 18 children (83%) showed a rise in ASAT values and 11 (61%) in ALAT values exceeding 29U/L. Seven children with maximal ASAT values between 40 and 100 U/L were treated without any changes in the regimen and the transaminases normalized later in the treatment. Six out of the eight children with ASAT values over 100 U/L were allowed a three-week pause in their therapy, one was given the same dose of rifampicin, and in one the treatment was discontinued entirely. The therapy was discontinued in an additional three children because of a second high rise in the transaminase values. Liver injury can occur at any time during treatment, and thus makes continuous follow-up tests necessary.

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Section: Discussionsupporting

confidence: 56%

Section: Discussionmentioning

confidence: 58%

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Hepatotoxicity of rifampicin and isoniazid in children treated for tuberculosis

Linna

Uhari

1980

Eur J Pediatr

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“…Increased levels of SGOT and SGPT are observed in conditions such as hepatitis, cirrhosis, obstructive jaundice and other hepatic diseases (Lal et al, 1972;Carlisle & Galambos, 1979). Significant increase in SGOT levels and SGPT levels were found post oral administration of RM (Tables 2 and 3, respectively).…”

Section: Phagocytosis Activity and Generation Of Nomentioning

confidence: 93%

Microparticles of rifampicin: comparison of pulmonary route with oral route for drug uptake by alveolar macrophages, phagocytosis activity and toxicity study in albino rats

Parikh¹,

Patel

Dalwadi³

2013

Drug Delivery

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Context: Tuberculosis (TB) is a chronic infectious disease with increasing incidence of drug resistance. Oral treatment for TB and multidrug resistance (MDR)-TB can have serious side effects. The causative agent of TB, Mycobacterium tuberculosis, resides in alveolar macrophages (AM). Pulmonary administration of anti-TB drugs can help in delivery of high concentration to AM. The ability of AM to phagocytose can also be utilized to generate mycobactericidal nitric oxide (NO) to improve efficacy of anti-TB drugs. Objective: To compare the uptake of rifampicin (RIF) by AM post oral and pulmonary administration of RIF microparticles (RM) and to compare hepatotoxicity and phagocytosis activity. Materials and Methods: RM were produced by spray drying process. RM were administered to rats through oral as well as intratracheal route. The uptake of RIF by AM and liver was measured. NO was measured in bronchoalveolar lavage (BAL) fluid. SGOT and SGPT levels were measured in serum. Results: Significantly higher (p50.05) concentration of RIF was found in AM post intratracheal administration. NO production was also significantly higher but less than toxic level. SGOT and SGPT levels as well as uptake of RIF by liver were indicative of no hepatotoxicity post intratracheal administration. Discussion: Phagocytosis of RM post intratracheal administration leads to significantly higher drug level in AM as well as production of significantly higher levels of NO. Conclusion: The administration of RM as dry powder inhalation (DPI) formulation may reduce treatment time of TB and chances of drug resistance TB.

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“…Second, the potential of isoniazid-mediated reactions seems to rise, when other drugs such as PAS or rifampin are given concomitantly. [8][9] Third, isoniazid-induced hepatotoxicity may be related to the individual's capacity to acetylate and excrete the drug.33 Acetylation of isoniazid is the major pathway of detoxification in the rhesus monkey34 and in man. 35 The ability of man to acetylate isoniazid is probably genetically con¬ trolled,1 eg, some individuals are "slow" and others "rapid" inactivators of the drug.1-33-36 The slow-inactivator character is probably inher¬ ited as an autosomal recessive,1 and seems more frequent among Cauca¬ sians137 and North American blacks,1 and less frequent in the Japanese,38 North American Indians, and Es¬ kimos.35…”

Section: Commentmentioning

confidence: 99%

Isoniazid Administration and Liver Injury

Rudoy¹

1973

Arch Pediatr Adolesc Med

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Isoniazid has been recognized as a cause of liver dysfunction in some patients receiving antituberculous therapy. The medical literature contains reports of isoniazid-induced hepatic injury in adults, but essentially none in children. We used this drug to treat a 6\ x =r eq-\ year-old Caucasian boy for active tuberculosis, and he suffered a reaction characterized by high fever, a morbilliform exanthem, peripheral eosinophilia, enlargement of the liver, and abnormal liver function and histologic findings. The histologic appearance of the liver lesion and the clinical manifestations were suggestive of a hypersensitivity reaction, probably of the delayed type.

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Effect of Rifampicin and Isoniazid on Liver Function

Cited by 56 publications

References 11 publications

Hepatotoxicity of rifampicin and isoniazid in children treated for tuberculosis

Hepatotoxicity of rifampicin and isoniazid in children treated for tuberculosis

Microparticles of rifampicin: comparison of pulmonary route with oral route for drug uptake by alveolar macrophages, phagocytosis activity and toxicity study in albino rats

Isoniazid Administration and Liver Injury

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